The first longitudinal multiprobe μPET study in a NMDAR hypofunction rat model.
Chronic high glutamate tends to upregulate mGluR5 expression or shift the affinity.
Microglial activation appears to amplify already increased glutamate levels.
TRYCAT pathway overactivation contributes to the pathology.
Targeting mGluR5 receptors for antipsychotics development remains promising.